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2 Pathological Processes > 11 Cell Adaptations > Flashcards

11 Cell Adaptations Flashcards

1
Q

What is aplasia?

A

Complete failure of specific tissue/organ to develop(proliferate)= embryonic developmental disorder

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2
Q

What would thymic aplasia result in?

A

Infections and autoimmune problems

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3
Q

What molecules regulate normal cell proliferation? (in general terms)

A

Proto-oncogenes

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4
Q

What are the 4 main phases of the cell cycle?

A

G1-S-G2-M

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5
Q

What happens at G0 of the cell cycle?

A

After M- cell undergoes terminal differentiation- permanent exit from cell cycle

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6
Q

How does the body increase the growth of a tissue?

A

-Shortening cell cycle -Converting quiescent cells (retained ability to divide)- proliferating cells

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7
Q

What happens during G1?

A

Cell grows

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8
Q

What happens during S phase?

A

DNA synthesis

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9
Q

What happens during G2 phase?

A

Cell prepares to divide (e.g. protein synthesis

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10
Q

What is the Restriction (R) Point?

A

At end of G1- Critical checkpoint (for DNA damage)

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11
Q

How many checkpoints are there in the cell cycle?

A

3

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12
Q

What is the p53 protein?

A

If checkpoint activation occurs- protein suspends cell cycle-triggers DNA repair mechanisms/apoptosis

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13
Q

Apart from the R Point, where are the other 2 major checkpoints in the cell cycle?

A

G1/S and G2/M

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14
Q

What are the proteins which regulate the cell cycle?

A

Cyclins CDKs CDK inhibitors

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15
Q

How do activated CDKs drive the cell cycle?

A

Phosphorylating proteins

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16
Q

What is the main protein which gets phosphorylated to drive the cell cycle?

A

Retinoblastoma Susceptibility Protein (RB Protein)

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17
Q

How do growth factors have an affect on the cell cycle?

A

-Stimulating cyclin production -Inhibiting production of CDK inhibitors

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18
Q

Define ‘Cell Adaptation’

A

State between normal unstressed cell and overstressed injured cell

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19
Q

What is Hyperplasia?

A

Increase in cell number (increasing tissue and organ size)

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20
Q

What may cause cell hyperplasia? (in general terms)

A

1-Increased functional demand (e.g. stimulated hormonally) 2-External Stimulation (Stimulated by damage=compensatory)

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21
Q

In what type of cell populations does hyperplasia occur?

A

Labile Stable

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22
Q

Is hyperplasia reversible?

A

Yes ( it is under physiological control)

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23
Q

How is hyperplasia different from regeneration?

A

Leads to increase in cell number

24
Q

What might cause pathological hyperplasia?

A

1-Excessive hormonal stimulation 2-Excessive GF production

25
Q

Why is neoplasia a risk in hyperplastic tissue?

A

Repeated cell divisions- increases risk of mutations

26
Q

Give an example of physiological hyperplasia.

A

-Increased bone marrow due to hypoxia- increased erythropoietin -Proliferation of endometrium due to oestrogen

27
Q

Give an example of pathological hyperplasia.

A

-Epidermal thickening due to chronic eczema -Enlargement of thyroid gland- iodine deficiency

28
Q

What is Hypertrophy?

A

Increase in cell size (increasing tissue and organ size)

29
Q

In which cell population is cell hypertrophy usually seen?

A

Permanent cell population (limited replicative potential)

30
Q

What may cause hypertrophy? (in general terms)

A

1-Increased functional demand 2-Hormonal stimulation

31
Q

What is the usual stimulus for a combination of hypertrophy and hyperplasia to occur?

A

Endocrine stimulation

32
Q

Give an example of physiological hypertrophy.

A

1- Skeletal muscle (body builder) 2-Smooth muscle- pregnant uterus (under oestrogen influence)

33
Q

Give an example of pathological hypertrophy.

A

1-Ventricular cardiac muscle hypertrophy (due to hypertension/valvular disease) 2-Smooth muscle hypertrophy- intestinal stenosis

34
Q

How do hypertrophy and hyperplasia differ from neoplasia?

A

Cells/tissues return to normal size when stimulus removed in hypertrophy/hyperplasia

35
Q

What is ‘atrophy’?

A

Shrinkage in cell size (cell atrophy) (reduces its function) Shrinkage in cell number (tissue atrophy) (at point where survival=still possible)

36
Q

What causes atrophy (in general terms)?

A

1-Reduced GF supply 2-Reduced nutrient supply

37
Q

In organs undergoing atrophy, which cell type will go first?

A

Parenchymal stem cells before stromal cells (so often lots of CT in atrophic organs)

38
Q

Give an example of where atrophy can be linked with senescence.

A

Atrophy of hair follicles- baldness

39
Q

Is atrophy reversible?

A

Up to a point in some cases (less so when parenchymal cells = replaced by CT)

40
Q

What’s the best way to treat atrophy?

A

Remove the cause

41
Q

Give an example of physiological atrophy.

A

-Ovarian atrophy- post menopause - Decreased uterus size- after parturition

42
Q

Give an example of causes of pathological atrophy.

A

-Reduced functional demand e.g. muscle disuse in a cast -Loss of innervation (motor nerve) -Inadequate blood supply (prolonged)= tissue death -Inadequate nutrition -Loss of endocrine stimulation -Persistent injury- e.g. polymyositis -Senile atrophy -Pressure e.g. tissues around benign tumour e.g. cerebral -Occlusion of secretory duct e.g. in pancreas -Toxic agents/drugs e.g. bone marrow -X-rays -Immunological mechanisms

43
Q

What is metaplasia?

A

Reversible replacement of one adult differentiated cell by another. (expression of new genetic programme)

44
Q

In what types of cells does metaplasia occur?

A

Varieties of: -Epithelia -Connective Tissue Only in populations that CAN REPLICATE

45
Q

In general terms, why does metaplasia occur?

A

Change one type of cell to another more suited to altered environment. (e.g. columnar epithelium–> squamous epithelium

46
Q

How does metaplasia differ from dysplasia?

A

Metaplasia- cells= fully differentiated Dysplasia- cells= disorganised + abnormal differentiation BUT metaplasia= sometimes prelude to dysplasia/cancer

47
Q

Give an example in which metaplasia can be useful.

A

Bone marrow destroyed due to disease- splenic tissue to bone marrow

48
Q

Give an example of pathological metaplasia.

A

Cigarette smoke- columnar epithelium–>stratified squamous epithelium. Lacks mucociliary escalator.

49
Q

What is ‘Barrett’s oesophagus’?

A

Flat, non-secreting epithelia=replaced by secretory epithelium/glands w./ persistent acid reflux

50
Q

What is ‘Traumatic myositis ossificans’?

A

Fibroblasts in muscle tissue change to osteoblast- after trauma- metaplastic bone develops in muscle

51
Q

What is hypoplasia?

A

Congenital underdevelopment/incomplete development of tissue/organ (inadequate cell number) =(spectrum w./ aplasia)

52
Q

What is atresia?

A

‘No orifice’ - congenital imperforation of opening e.g. anus/vagina

53
Q

How is regeneration different from reconstitution?

A

Reconsitution= replacement of lost body part rather than small group of cells

54
Q

What is ‘Involution’?

A

Normal, programmed shrinkage of organ (overlaps w./ atrophy)

55
Q

Give an example of involution occurring in the body.

A

-Uterus after child birth

56
Q

What is dysplasia?

A

Abnormal maturation of cells in tissue- often pre-cancerous condition

2 Pathological Processes (12 decks)

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